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Takashi Yamamura

Researcher at Nagoya University

Publications -  264
Citations -  13059

Takashi Yamamura is an academic researcher from Nagoya University. The author has contributed to research in topics: Natural killer T cell & Experimental autoimmune encephalomyelitis. The author has an hindex of 63, co-authored 239 publications receiving 11771 citations.

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A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells.

TL;DR: A synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14+) is preventive against EAE and targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.
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Dysbiosis in the gut microbiota of patients with multiple sclerosis, with a striking depletion of species belonging to clostridia XIVa and IV clusters

TL;DR: Analysis of the bacterial 16S ribosomal RNA (rRNA) gene by using a high-throughput culture-independent pyrosequencing method provided evidence of a moderate dysbiosis in the structure of gut microbiota in patients with MS, and phylogenetic tree analysis revealed that many of the clostridial species associated with MS might be distinct from those broadly associated with autoimmune conditions.
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Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica

TL;DR: It is demonstrated that a B-cell subpopulation, exhibiting the CD19intCD27highCD38highCD180− phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies are mainly produced by these cells in the blood of these patients.
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Modulation of CD1d-restricted NKT cell responses by using N-acyl variants of α-galactosylceramides

TL;DR: It is reported that substituting the C26:0 N-acyl chain of KRN7000 with shorter, unsaturated fatty acids modifies the outcome of Valpha14i NKT cell activation, and one analogue containing a diunsaturated C20 fatty acid potently induced a T helper type 2-biased cytokine response.